Chronic & cancer pain

Overview & definition

The chronic pain is the pain persisting beyond the normal healing time (over 3 months), distinct from the acute pain in the mechanisms, the psychology, and the management. The cancer pain is the pain of the malignancy (the tumour invasion, the nerve involvement, the treatment-related). Both are prevalent, disabling, and complex — the biopsychosocial conditions requiring the multidisciplinary management. The pain medicine is a recognised specialty (the FFPM in Australia and New Zealand, the FIPP globally); the anaesthetist is a key member of the pain team and the provider of the interventional techniques.[1][2]

The pain types — the nociceptive, the neuropathic, the nociplastic

The pain is classified by the mechanism:[1]

• The nociceptive pain — the activation of the nociceptors by the tissue damage (the inflammatory, the mechanical, the ischaemic). The somatic (the bone, the muscle, the skin — the well-localised, the aching, the sharp) and the visceral (the organs — the poorly localised, the dull, the referred). Responds to the anti-inflammatory and the opioid analgesia.
• The neuropathic pain — the lesion or the disease of the somatosensory nervous system (the diabetic neuropathy, the postherpetic neuralgia, the sciatica, the phantom limb, the central post-stroke pain). The burning, the shooting, the electric, the allodynia (the pain from the non-painful stimulus), the hyperalgesia. Responds to the gabapentinoids, the SNRIs, the TCAs — NOT the opioids alone.
• The nociplastic pain — the altered nociception despite the no clear tissue damage or the nerve lesion (the fibromyalgia, the complex regional pain, the irritable bowel, the chronic primary pain). The central sensitisation. The management is the multidisciplinary, the psychological, and the selected pharmacology. [1]

The mixed pain (the nociceptive plus the neuropathic) is common, especially in the cancer and the chronic back pain.[1]

The central sensitisation and the chronic postsurgical pain

The chronic pain is underpinned by the central sensitisation — the amplified signalling in the dorsal horn and the brain after the sustained or the repeated nociceptive input, lowering the threshold and amplifying the response. The chronic postsurgical pain (the CPSP) is the chronic pain developing after the surgery (the breast, the thoracic, the hernia, the amputation) in up to 10 to 50 per cent of the patients, driven by the nerve injury, the acute postoperative pain, the psychological factors, and the genetic predisposition. The somatic and the psychological predictors (the preoperative pain, the anxiety, the depression, the catastrophising) are identified to target the prevention. The perioperative multimodal analgesia, the regional techniques, and the psychological preparation reduce the CPSP.[6]

The cancer pain — the WHO analgesic ladder

The cancer pain is prevalent (the 30 to 70 per cent of the cancer patients, higher in the advanced disease). The WHO analgesic ladder (the three-step framework): (1) the non-opioid (the paracetamol, the NSAID) for the mild pain; (2) the weak opioid (the codeine, the tramadol) for the moderate; (3) the strong opioid (the morphine, the oxycodone, the fentanyl) for the severe — with the adjuvants at each step. The ladder has guided the global cancer-pain management for the decades, though the modern evidence questions the routine paracetamol add-on (the PaSo trial found the no benefit of the paracetamol added to the strong opioids for the cancer pain).[4]

The cancer pain is often mixed (the nociceptive bone pain, the neuropathic nerve-invasion pain, the visceral). The pancreatic cancer pain (the celiac-plexus involvement) is the classic severe neuropathic-visceral pain warranting the early interventional approach (the celiac plexus block) alongside the pharmacology.[2]

The neuropathic pain pharmacotherapy

The first-line agents for the neuropathic pain (the NeuPSIG and the NICE guidance):[1]

• The gabapentinoids (the gabapentin, the pregabalin). The alpha-2-delta calcium-channel ligands. The pregabalin (the linear pharmacokinetics, the twice-daily dosing) is the common choice; the consensus on its clinical use in the peripheral neuropathic pain guides the dosing and the titration. The adverse effects: the sedation, the dizziness, the weight gain, the oedema; the dependence and the misuse risk. The dose-adjusted in the renal impairment.
• The SNRIs (the duloxetine, the venlafaxine). The serotonin-noradrenaline reuptake inhibitors. The duloxetine is the first-line for the painful diabetic neuropathy and the fibromyalgia.
• The TCAs (the amitriptyline, the nortriptyline). The effective but the anticholinergic and the cardiac adverse effects limit the use, especially in the elderly. [1]

The second-line: the lidocaine patches (the localised), the capsaicin patch (the localised), the tramadol. The strong opioids and the cannabinoids are the third-line or the selected cases. The combination of the different-mechanism agents is the principle.[1]

The chronic opioid therapy and its risks

The chronic opioid therapy for the non-cancer pain is the contentious area — the limited long-term benefit, the substantial risks. The adverse effects: the dependence and the tolerance, the opioid-induced hyperalgesia (the paradoxical pain increase), the endocrine effects (the hypogonadism, the infertility), the immune suppression, the constipation, the sedation, and the overdose and the death risk. The opioid epidemic underscored the harm. The modern guidance: the chronic opioid only for the selected patients (the severe pain, the failed alternatives), the lowest effective dose, the regular review, the risk stratification, the monitoring, and the tapering where the benefit is lost. The cancer-pain opioid use is the different context (the life-limiting disease, the analgesia-first) but the opioid stewardship still applies.[4]

The cancer pain — the interventional techniques

The interventional techniques are the adjuncts for the refractory cancer pain:[2][3]

• The neurolytic blocks. The chemical (the alcohol, the phenol) or the thermal destruction of the pain pathway. The celiac plexus block for the pancreatic and the upper-abdominal cancer pain; the splanchnic, the superior hypogastric, the ganglion impar for the visceral pain. The neuraxial neurolysis for the sacral pain. The benefit-duration variable, the neurological risk.
• The peripheral nerve stimulation. The targeted stimulation of the peripheral nerve (the newer modality, with the emerging role in the perioperative and the cancer pain).[3]
• The radiofrequency ablation. The thermal lesioning of the medial branch for the facet-joint pain, and the other targets.
• The trigger point injections and the joint injections. For the musculoskeletal pain.

The neuromodulation — the spinal cord stimulation and the intrathecal drug delivery

The neuromodulation is the targeted delivery of the electrical or the pharmacological stimulus to the nervous system for the refractory chronic pain:[5]

• The spinal cord stimulation (the SCS). The implanted epidural leads deliver the electrical pulses (the tonic, the burst, the high-frequency) that modulate the dorsal-column and the dorsal-horn signalling, reducing the chronic neuropathic pain (the failed back surgery syndrome, the complex regional pain, the painful diabetic neuropathy, the ischaemic pain). The patient selection (the trial stimulation), the programming, and the long-term management are the keys. The intrathecal drug delivery is the rescue strategy in the patients with the inadequate SCS response.[5]
• The intrathecal drug delivery (the IDD). The implanted pump delivers the opioid (the morphine, the hydromorphone), the local anaesthetic (the bupivacaine), the clonidine, the ziconotide, and the baclofen directly to the spinal cord, achieving the high spinal effect with the low systemic dose. The IDD is for the refractory cancer and the selected chronic non-cancer pain. The rescue-IDD role in the SCS-failure patients is the recognised.[5]
• The dorsal root ganglion stimulation. The newer modality for the focal neuropathic pain.

The multidisciplinary biopsychosocial management

The chronic pain is the biopsychosocial condition — the biological, the psychological, and the social factors interact. The management is the multidisciplinary: the medical (the pharmacology, the interventions), the psychological (the CBT, the ACT, the acceptance, the pain education, the management of the depression and the anxiety), the physical (the exercise, the physiotherapy, the graded activity), and the social (the vocational, the relationships, the social support). The pain-medicine programme (the intensive, the multidisciplinary) improves the function and the quality of life. The goal is the function and the quality of life (the not the complete pain relief — the often-unrealistic).[6]

The pain assessment

The pain assessment is the biopsychosocial. The pain history (the onset, the character, the severity, the aggravators, the relievers), the functional impact (the activities, the sleep, the work, the relationships), the psychological state (the mood, the anxiety, the catastrophising, the coping), the social context (the work, the family, the stressors), the past treatments, and the physical examination. The validated tools (the DN4 and the painDETECT for the neuropathic screening; the Brief Pain Inventory for the cancer pain; the Oswestry for the back pain; the psychological scales). The assessment informs the individualised plan.[1][2]

The patient with the chronic pain and the surgery

The patient with the chronic pain presenting for the surgery is the high-risk for the postoperative pain (the central sensitisation, the opioid tolerance, the anxiety). The perioperative plan: the continuation of the baseline analgesia, the multimodal opioid-sparing analgesia (the regional, the ketamine, the gabapentinoid), the pain-medicine liaison, the realistic expectations, and the transition plan. The peripheral nerve stimulation and the regional techniques have an emerging perioperative role in the cancer surgical patient.[3][6]

The palliative and the end-of-life care

The cancer pain at the end of life requires the compassionate, the effective, and the individualised management. The opioids (the morphine, the oxycodone, the fentanyl, the methadone), the adjuvants (the neuropathic, the bone, the visceral), the interventions (the neurolytic blocks, the intrathecal), and the holistic care (the psychological, the social, the spiritual) are the components. The palliative care team is the partner. The goal is the comfort and the dignity.[2][4]

The FFPM and the pain medicine specialty

The pain medicine is a recognised specialty. The Faculty of Pain Medicine (the FFPM ANZCA, the FIPP) is the specialist qualification. The pain physician (the anaesthetist, the neurologist, the rehabilitation physician, the GP with the special interest) leads the pain team (the pain nurse, the physiotherapist, the psychologist, the pharmacist). The chronic-pain management is the specialised, the multidisciplinary practice, distinct from the acute anaesthetic pain service.[1][6]

[1] [1]

Red flags

[1] [1] [1] [1] [1]

References

1. [1]Lu H, et al. Consensus on the Clinical Use of Pregabalin in Peripheral Neuropathic Pain CNS Neurosci Ther, 2026.PMID 42310848
2. [2]Blero D, et al. Pain management in pancreatic cancer: time to change our strategy! Curr Opin Oncol, 2026.PMID 42240215
3. [3]Johnson T, et al. Peripheral Nerve Stimulation for Perioperative Care in Oncologic Surgical Cases: A Narrative Review Healthcare (Basel), 2026.PMID 42354627
4. [4]Hagen KMR, et al. PaSo paracetamol with strong opioids trial: paracetamol versus placebo in conjunction with strong opioids for cancer pain-a pilot randomised placebo-controlled withdrawal trial BMJ Support Palliat Care, 2026.PMID 42309698
5. [5]Cordero-Tous N, et al. Intrathecal Drug Delivery as a Rescue Strategy in Patients with Spinal Cord Stimulation: A Single-Center Case Series J Clin Med, 2026.PMID 42355686
6. [6]Sperandio G, et al. Somatic and psychological predictors of chronic postsurgical pain in cancer patients: a machine learning approach in a longitudinal two-centre study Br J Anaesth, 2026.PMID 41506969